Transient global amnesia in legal proceedings.

Transient global amnesia (TGA) is a neurological disorder characterized by an acute onset of severe anterograde amnesia. While retrograde amnesia may be present-although to a lesser extent-patients have no further cognitive disturbances or neurological signs. These symptoms resolve fully within several hours leaving a permanent memory gap for the duration of the episode and do not lead to long-term neurological deficits. In addition to well-defined clinical diagnostic criteria, in up to 80 % of patients, small, point-shaped lesions in the hippocampus are detected 24-48 h after symptom onset on diffusion-weighted magnetic resonance images. Despite several etiological hypotheses, to date, there is no scientific proof for the etiology of TGA or the small hippocampal lesions. Interestingly, in a large number of cases, an emotionally or physically straining event precipitates the onset of TGA, suggesting a stress-related mechanism. We report two cases of TGA occurring in legally relevant settings: affecting the victim of brutal burglary and the key witness in a murder trial. In the context of forensic medicine, the knowledge of this disorder and recognition of its typical features are essential.

Stroke and cancer: the importance of cancer-associated hypercoagulation as a possible stroke etiology.

BACKGROUND AND PURPOSE: The importance of cancer-associated hypercoagulability as a possible stroke etiology in patients with cancer has received relatively little attention to date. A recent study has suggested that cancer-associated hypercoagulation may be of special importance in the absence of conventional stroke mechanisms. METHODS: We identified patients with ischemic stroke sequentially admitted to our stroke center with the additional diagnosis of active and malignant cancer from 2002 to 2011. By using our prospectively collected stroke, MRI, and laboratory data banks, the etiology and risk factors of stroke, types of cancer, deep vein thrombosis/pulmonary embolism, d-dimer levels, and diffusion-weighted imaging lesion patterns were compared to an age- and sex-matched control group. Patients with cancer with a conventional stroke etiology and patients with an unidentified and/or cancer-associated stroke etiology were analyzed separately. RESULTS: One hundred forty patients with cancer and 140 control subjects were included. Unidentified stroke (P<0.001) and infarction in multiple vascular territories (P<0.001) were significantly more frequent and d-dimer levels significantly higher (P<0.05) in patients with cancer. Vice versa, risk factors such as hypertension (P<0.05) and hyperlipidemia (P<0.01) were more prevalent in control subjects. Deep vein thrombosis and pulmonary embolism were more frequent (P<0.01) and d-dimer levels higher (P<0.01) in the patients with unidentified and/or cancer-associated stroke etiology compared to the patients with cancer with a conventional stroke etiology. Lung and pancreatic cancer were significantly overrepresented and d-dimer levels higher in these patients compared with other patients with cancer (P<0.01). CONCLUSIONS: Our data confirm the concept of cancer-associated hypercoagulation as a widely underestimated important stroke risk factor in patients with cancer, especially in those with severely elevated d-dimer levels and in the absence of conventional risk factors.

Predictors and early outcome of hemorrhagic transformation after acute ischemic stroke.

BACKGROUND: Hemorrhagic transformation (HT) after acute ischemic stroke is frequently detected using magnetic resonance imaging (MRI), in particular in patients treated with tissue plasminogen activator (tPA). Knowledge about causes and early clinical consequences of HT mostly arises from computed tomography-based studies. We analyzed potential predictors and early outcome of HT after stroke detected by MRI with T(2)*-weighted gradient echo sequences (T(2)*-MRI). METHODS: 122 consecutive stroke patients (mean age 65.5 years, 41% women) who underwent T(2)*-MRI within 6-60 h after stroke onset were included. 25.4% of patients were treated with tPA; the overall detection rate of HT on T(2)*-MRI was 20.5%. Potential predictors of HT, such as age, sex, blood pressure, stroke etiology, prior antithrombotic medication, neurological deficit on admission, tPA treatment, and specific MRI findings, were analyzed. In addition, we evaluated the effect of HT on early outcome: a decrease of >4 points on the National Institute of Health Stroke Scale (NIHSS) on day 5 was considered early improvement, and an increase of >4 points was considered early deterioration. RESULTS: The main predictor for occurrence of HT was tPA treatment (48.4 vs. 11.1%; odds ratio 7.50; 95% confidence interval 2.9-19.7; p < 0.001). Furthermore, the development of HT was associated with a severer neurological deficit on admission (mean NIHSS score 9.9 vs. 5.9; p = 0.003), and territorial infarction (88 vs. 58.8%; p = 0.007). 19 patients (15.6%) showed early improvement which was associated with the occurrence of HT (p = 0.011) and tPA treatment (p < 0.001). CONCLUSIONS: HT is a frequent finding on T(2)*-MRI in patients with acute ischemic stroke associated with tPA treatment, territorial infarction and severer neurological deficits on admission. However, HT does not cause clinical deterioration; it is rather related to a favorable early outcome likely reflecting early recanalization and better reperfusion in these patients.

Improved detection of intracerebral hemorrhage with transcranial ultrasound perfusion imaging.

BACKGROUND: Ultrasound perfusion imaging (UPI) is a new approach for the assessment of brain perfusion. In contrast to the increasing experience with this method in patients with ischemic stroke, data on the value of UPI for the diagnosis of intracerebral hemorrhage (ICH) are lacking. METHODS: We investigated 12 consecutive patients with sufficient temporal bone windows and a CT diagnosis of acute supratentorial ICH (basal ganglia n = 9 and lobar n = 3). Native transcranial B-mode ultrasound and UPI studies with echo contrast agents were performed on day 1 and on days 5-7 including volume measurements using the maximum extension on transverse and coronal ultrasound planes. RESULTS: ICH was identified as hyperechogenic mass on B-mode ultrasound in 11/12 patients, but the correlation with CT volume measurements was poor (day 1: r = 0.4, 95% confidence interval, CI: -0.23-0.79; p = 0.1; follow-up: r = 0.58, 95% CI: 0.04-0.86; p = 0.21). Volume measurement was more precise using UPI with a significant correlation on day 1 (r = 0.8, 95% CI: 0.47-0.94; p < 0.001) and during the follow-up (r = 0.94, 95% CI: 0.81-0.98; p < 0.001). Using UPI the typical finding was a focal reduction of contrast agent arrival in the ICH core which led to better delineation of the lesion borders from adjacent tissue. Depiction of lobar ICH was difficult with ultrasound, and lesion sizes tended to be underestimated. CONCLUSIONS: This study supports earlier work demonstrating the usefulness of native transcranial ultrasound for the diagnosis of ICH. UPI further improves diagnostic reliability and allows very precise ICH volume measurements. If confirmed in larger studies, this approach may be useful for bedside monitoring of ICH progression and regression.

Thrombolysis in patients with lacunar stroke is safe: an observational study.

Research suggests that the etiology of lacunar stroke is different from that of other stroke subtypes. This could imply an altered response to thrombolysis, but data concerning the efficacy of rt-PA in lacunar stroke is limited and inconsistent. From our prospectively collected stroke database, we identified patients with an MRI-confirmed purely lacunar stroke that were treated in our Stroke Unit between 2004 and 2011. We compared both the clinical course (NIHSS, deterioration, mRS at 3 months) and the MRI findings between patients who either received or did not receive rt-PA. In comparison to patients who obtained standard medical care (n = 468), acute lacunar stroke patients treated with rt-PA (n = 69) were more severely affected on admission (median NIHSS of 5 vs. 3; p < 0.001) and presented less frequently with a lacunar syndrome (74 vs. 88 %; p = 0.003). The clinical course was more favorable in patients treated with rt-PA (median NIHSS improvement of 3 vs. 1; p < 0.001), while functional deficit after 3 months was similar in both groups (median mRS of 2; p = 0.211). Overall complication rates did not differ significantly between the two groups, but while we did not detect symptomatic intracranial hemorrhage, hemorrhagic transformation was more frequent in thrombolyzed patients (11.6 vs. 1.9 %; p = 0.001). Patients with acute lacunar stroke benefited from thrombolysis without additional complications. Thus, patients with suspected acute lacunar stroke or lacunar syndrome should not be treated differently than other stroke populations.

Treatment with tPA predicts better outcome even if MCA occlusion persists.

BACKGROUND AND HYPOTHESIS: Functional improvement after middle cerebral artery ischaemia seems to depend on recanalization of large-vessel occlusion as early as possible. The only approved medical treatment for acute stroke is early IV tissue plasminogen activator administration. However, while some patients do not benefit from quick recanalization, others recover despite persistent middle cerebral artery occlusion. We wondered whether there are different effects of tissue plasminogen activator treatment on large artery and small artery reopening. METHODS: We enrolled 55 acute stroke patients who showed persisting middle cerebral artery occlusion evidenced by transcranial colour-coded duplex ultrasonography in follow-up examination within 48 h postonset of middle cerebral artery stroke syndromes (mean 30·8 ± 5·4 h after admission). Twenty-two of 55 had been treated with tissue plasminogen activator and 33/55 had been treated without tissue plasminogen activator. We compared neurological (National Institutes of Health Stroke Scale) and functional (modified Rankin Scale) scores at baseline, after seven-days, and then after two-months. Risk factors, previous stroke prophylaxis, as well as clinical baseline characteristics were analysed to exclude significant differences between both groups. RESULTS: Despite later admission to hospital (tissue plasminogen activator patients 1·6 ± 0·66 h vs. non-tissue plasminogen activator patients 7·4 ± 5·84 h; P < 0·001), there was no significant difference between both groups concerning demographic data, severity of symptoms on admission, risk factors, stroke prophylaxis, as well as basic laboratory values (international normalized ratio, leucocyte count, C-reactive protein) blood pressure and body temperature on admission. Irrespective of Doppler findings demonstrating persistent middle cerebral artery occlusion in all 55 patients, there was a significant neurological and functional improvement in tissue plasminogen activator patients compared to non-tissue plasminogen activator patients. Tissue plasminogen activator patients had a mean improvement on National Institutes of Health Stroke Scale within the first seven-days of 2·8 points, while non-tissue plasminogen activator patients deteriorated by 2·2 points (P < 0·001). Concerning modified Rankin Scale tissue plasminogen activator-treated patients showed a mean improvement within the first seven-days of 0·5 points, while non-tissue plasminogen activator patients deteriorated by 0·3 points (P = 0·019). A favourable overall short-term clinical course (i.e. improvement on National Institutes of Health Stroke Scale >3 points and/or modified Rankin Scale >1 point) was found in 36·4% of tissue plasminogen activator patients and in 6·1% of non-tissue plasminogen activator patients (P = 0·0047). At two-months follow-up, patients still showed a median modified Rankin Scale of 4 points after tissue plasminogen activator treatment and 5 points after non-tissue plasminogen activator treatment (P = 0·023). CONCLUSION: Although the prognosis of patients with persisting middle cerebral artery occlusion after tissue plasminogen activator administration is known to be poor, patients do better if treated with tissue plasminogen activator vs. those who could not be treated - mainly for late presentation. This may be due to sufficient small vascular territory recanalization despite persistence of large artery occlusion after tissue plasminogen activator treatment.

Real-time ultrasound brain perfusion imaging with analysis of microbubble replenishment in acute MCA stroke.

Real-time ultrasound perfusion imaging (rt-UPI) allows visualization of microbubbles flowing through the cerebral microvasculature. We hypothesized that analysis of microbubble tissue replenishment would enable for characterization of perfusion deficits in acute middle cerebral artery (MCA) territory stroke. Twenty-three patients (mean age 70.2 ± 13.2 years, 9 weeks) were included. Sequential images of bubble replenishment were acquired by transcranial rt-UPI at low mechanical index immediately after microbubble destruction. Different parameters were calculated from regions of interest (ROIs): real-time time to peak (rt-TTP), rise rate (ß), and plateau (A) of acoustic intensity, and A × ß was used as an index of blood flow. Results were compared with diffusion-weighted and perfusion magnetic resonance imaging. Parameters of rt-UPI had lower values in ROIs of ischemic as compared with normal tissue (ß=0.58 ± 0.40 versus 1.25 ± 0.83; P=0.001; A=1.44 ± 1.75 versus 2.63 ± 2.31; P=0.05; A × ß=1.14 ± 2.25 versus 2.98 ± 2.70; P=0.01). Real-time time to peak was delayed in ischemic tissue (11.43 ± 2.67 versus 8.88 ± 1.66 seconds; P<0.001). From the analysis of receiver operating characteristic curves, ß and A × ß had the largest areas under the curve with optimal cutoff values of ß<0.76 and A × ß<1.91. We conclude that rt-UPI with analysis of microbubble replenishment correctly identifies ischemic brain tissue in acute MCA stroke.